Longevity researches at Harvard University

 

This is a part of sinclair lab researches at Harvard University about longevity:

1) Reprogramming cells to be young again

Our work has led us to the conclusion that the loss of epigenetic information is likely the root cause of aging. By analogy, if DNA is the digital information on a compact disc, then aging is due to scratches. We are searching for the polish. Our work has led us to identify reprogramming factors that we believe will enable us to reset a cell’s epigenetic status and reverse its age. We have developed human-compatible viral vectors to deliver the reprogramming genes to specific tissues or the entire body, thereby causing cells to act younger and wounds to heal faster. Our current focus is on nerve regeneration and the reversal of other symptoms of aging. We see treatments being possible for companion animals and humans to dramatically improve their health and lifespan.

So conclusion: research has found the cause of aging and now they are working on it mainly on the regeneration of nerve cells.

nerve regeneration

2) Can we develop drugs that slow aging?

Our work on SIRT1 led us to an exciting finding that the level of nicotinamide adenine dinucleotide (NAD+), cofactor of SIRT1, declines with age. We study the mechanisms by which the NAD+ level affects DNA repair and look for therapeutic targets to improve this process. In particular, we focus on delineating the biology of NAD+-depleting and producing enzymes as direct tools to control the NAD+ level in the cells toward increased health-span and improved physiological resilience.

 

The discovery of longevity genes showed that it is possible to greatly slow the pace of aging and disease by manipulating just one central pathway. This raises the possibility that we can find small molecules that can treat multiple, seemingly unrelated diseases, with a single medicine. Our lab has been highly active in this area, starting with the discovery of sirtuin activating compounds (STACs) in 2003. Since then, potent activators have been discovered and some of these are now in clinical trials, producing positive results. We have active studies to understand how STACs work at the molecular and the physiological levels using cutting-edge enzymological and structural methodologies and mouse genetic models in which we can delete genes at any time throughout the lifespan of the animal, and in specific organs. We published, for example, that the ability of resveratrol and a STAC called SRT1720 to increase mitochondrial function, require the SIRT1 gene in vivo. We have an active program to develop novel molecules that raise NAD levels. We are testing them for their effects on aging and age-related diseases. Human clinical trials with NAD-boosting molecules are ongoing.

in conclusion research has identified a molecule that has a relationship with aging (NAD+) research is still in progress on this molecule, and apparently there are tests on molecules capable of influencing NAD+ levels in blood.

 

 Improving Health Through NAD+ Boosting